Otitis 3: Eksterna - Patofisiology

Patofisiology
Trauma to the ear hole, the accumulation of keratin, or changes in pH can affect the occurrence of inflammation and infection. One study revealed that the bacteria have aerobe share of 91%, anaerobe four percent (4%), and also a mix of infection-four percent (4%). Organism is found most often among others have Pseudomonas aeruginosa (50%), Staphylococcus aureus (23%), anaerobe and gram negative organisms (12.5%), and yeast such as Aspergillus and Candida (12.5%). Increase of pH of pond water can be trusted to make infection may be more severe.

Predispositions Factors
Factors specific predisposes as follows:
a. Changes in skin pH is usually acid canalise be bass.
b. Changes in the environment, especially a combination of increased temperature and humidity.
c. A trauma is often mild or swim because of excessive ear cleaning.

Symptom and alert
Symptoms arising in otitis external diffuse, among others:
a. Redness on the outside of the ear (pinna) and ear hole that used to feel very sore.
b. Scaly skin that is good in and around the ear hole when flake.
c. Discharge from the ear and a little thin like pus.
d. Droop when the ear or jaw
e. At the time of ingest felt pain in the throat
f. Some people also lost their hearing

A diagnostic
a. Press painful tragus
b. Great pain
c. Most of the swelling wall canalise
d. Secret slightly
e. Hearing normal or slightly reduced
f. The absence of a fungus disease
g. There may be a painful adenopati regional press

Otitis external diffuse usually very painful
Stroma covering the bones in the third hole in the ear is very thin so that it allows only minimal swelling. So subjective interference experienced patients are often not comparable with that observed disease investigator.


Clinical manifestations
Eritema skin, secret a greenish skin edema and ear hole is a classical signs of otitis diffuse acute. Stench of secret not occur. Otitis external diffuses can be divided into 3 stages, namely:

a. Stadium "Pre inflammatory"
Stadium began with the loss of this layer of fat is normal and can be caused by the entry of water during the swim, wear clean cotton wool, and pry into your ear hole with the tools blunt. When the fat layer disappears at the time the weather is hot and humid air from the womb corneum increased stratum so that edema occurred intracellular. Edema is caused secret expenditure through orifisum apopilosebasea and layers of fat.
When exposed to hot and humid weather and long time the skin of the ear hole is not protected masers experience and reasonable ekfoliasi of cells epistle of the stratum corneum will not occur. This will cause a tickle, so try to minimize it with a paw or rub the cycle until there were: itching, Lucifer (itch scratch cycle). This will cause trauma to the stratum corneum, and there were predisposes for infection.

b. Stadium acute inflammation
Stadium this happens in 3 levels, namely: light, medium and heavy.
1. Lightweight
At the stadium, the patient experienced malaise when the light touches the tragus or concha moving. On examination the ear skin vagina will appear eritema and edema. When found a layer of clear secret not smell or accumulation of materials rekfoliasi or both. Ear drum looks less shiny.
2. Medium
Found itchiness and pain that are. Lumen ear hole partially closed by edema and exudate. Appear mass "debris" seropurulen cover the lumen and edema can also be seen there is currently little auricular, but does not have adenopati.
3. Heavy
On a more serious cases, patients complain of severe pain when chew and manipulated outside the ear. Although the helix does not seem involved, have found a clear edema periaurikuler and closing the lumen of the ear hole. Secret seropurulen a gray or green and exfoliated the visible mass in the lumen. Skin of the ear hole appear edema, and thick as can be seen papula, especially on top of the rear wall.
There is a decrease in the characteristics of the skin on the wall behind your ear hole (convex sagging), with a smooth and convex. This decrease extends membrane tympani. Otoskopi on using the enlargement, then can be seen papula white milk protruding from the surface and the surface, can also vesicle grayish organized by regions eritema.
Histopatologi showed the infected epidermis, and edema. Gram negative bacillus mainly pseudomonas species culture can almost 100% of your ear like this. When infected solved, it will appear papula small and pustule arising from secret purulent. In many circumstances this neutrofil complications can be obtained from the results secrete undelete it.

c. Stadium chronic infections (inflammation chronicles)
Besides the ear skin of leaves vary in degree, will thick (hiperkeratosis, acanthuses) and edema, which extends into the ear so that will orificium going refinement of the vagina and the ear hole of the ear, and abrasions on the laserasi lobe and conch. Dry mass and exfoliated often closed ear hole and can be found also secret colored gray or brown greenish and the smell fills recesses timpani.
Ear drum is not shiny and thick. Culture of the ear hole would result in the growth of gram negative bacillus (especially Proteus) and sometimes found fungi. Undelete will showed that the colored cells epistle basil and a very large amount.

Histopatology
In the acute otitis external diffuse the picture looks hiperkeratosis epidermis, parakeratosis, acanthuses, erosion, spingiosis, hiperplasia stratum corneum and stratum germinativum, edema, hiperemis, infiltration leukocyte, necrosis, necrosis focal followed in the dermis of healing fibroblast and apparatus gland decreased, the activities secretaries gland reduced.

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Peritonsiler abscess (PTA / Quinsy) 8

Management
Handling peritonsiler abscess include hydration, pain, and antibiotics are effective to overcome Staphylococcus aureus and anaerobic bacteria. Fine needle aspiration is an effective treatment in 75% peritonsiler abscess in children and is recommended as primary therapy unless there is a history of recurrent tonsillitis, or abscess before it peritonsiler measure is immediately tonsilektomi (Bailey, 2005).
In the infiltration stage, given high doses of antibiotics, and symptomatic medications. Also need to gargle-gargle with warm water and cold compresses on the neck. Appropriate choice of antibiotic depends on the results of cultures of microorganisms in the needle aspiration. Penicillin is a "drug of choice" in peritonsilar abscesses and 98% effective in cases when the combicated with metronidazole. Dosage for penicillin in adults is 600 mg IV every 6 hours for 12-24 hours, and children 12500-25000 U / kg every 6 hours.
Initial dose metronidazole for adult maintenance dose of 15mg/kg and 6 hours after initial dose with intravenous 7.5 mg / kg for 1 hour was given for 6-8 hours and not exceed 4 grams / day (Fachruddin, 2002).
If formed abscess, requiring surgical drainage, either by needle aspiration technique or with incision and drainage techniques. Difficulties may arise in ascertaining whether associated with acute cellulitis or abscess formation which had actually been hesitant happen, needle size 17 can be inserted (after application with anesthetic spray) into the three locations that seemed most likely to produce pus aspirations. If pus is found by accident, this method may be sufficient for drainage followed by antibiotics. If the amount of pus were found, and insufficient drainage with this method, a further incision and drainage can be done (Adams, 1997).
Incision and drainage technique requires local anesthesia. First pharynx sprayed with topical anesthetic. Then 2 cc Xilocain with adrenaline 1 / 100, 000 injected. Knife tonsila no 12 or no 11 with tape to prevent deep penetration used to make the incision through the mucosa and submucosal polar near the tonsilaris fossa. Place of incision is the most prominent areas and soft or in the middle of the line joining the base of uvula with the last molar on the side of dull aching Hemostat is inserted through the incision and gently stretched. Tonsila suction should be provided to collect pus issued. In older children or young adults with severe trismus, surgical drainage for abscesses peritonsiler possible after the application of fluid cocaine 4% in the incision area and regional areas and the fossa ganglion sfenopalatina Nasalis. This is sometimes reduce pain and trismus. Children younger require general anesthesia. Tonsilektomi recommends immediate (tonsilektomi quinsy) feel that this is a safe procedure that helps perfect drainage of the abscess if tonsila removed (Adams, 1997).
When tonsilektomi performed with acts of abscesses drainage tonsilektomi it is called "a chaud", when tonsilektomi performed 3-4 days after darinase abscess tonsilektomi called "a tiede" and if tonsilektomi performed 4-6 weeks after the drainage of abscesses tonsilektomi called "a froid ". Tonsilektomi generally performed after the infection quiet, ie 2-3 weeks after the drainage of abscesses (Fachruddin, 2002).
If there is trismus, then to overcome the pain, given analgesia (local), with novocain injected xylocain or 1% of ganglion sfenopalatinum. This ganglion is located at the rear of the lateral from concha media. Sfenopalatinum ganglion nerve has branches Palatina anterior and posterior media that send branches to aferen nerve tonsil and palate molle on the tonsils. The most appropriate area for the incision got inervasi from Palatine branch m. trigeminal ganglion sfenopalatinum passing. Then the patients recommended for surgery tonsilektomi (Fachruddin, 2002).
Tonsilektomi an absolute indication to people who suffer from recurrent abscess or abscess peritonsilaris which extends to the surrounding tissue. Peritonsil abscess has a large tendency to relapse. Until now there has been no agreement on when tonsilektomi done peritonsil abscess. Some authors recommend 6-8 weeks later tonsilektomi considering the possibility of bleeding or sepsis, whereas others recommend immediate tonsilektomi (Adams, 1997).

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Peritonsiler abscess (PTA / Quinsy) 7

DIAGNOSIS
Information from patients is needed to make the diagnosis peritonsiler abscess. Patients had a history of pain in the esophagus is one that supports peritonsilar abscess. History of acute pharyngitis and tonsillitis accompanied by a lack of comfort in unilateral pharingeal (Steyer, 2007).
The diagnosis is rarely in doubt if the inspector saw a large swelling peritonsilaris, pushing past the midline uvula, with edema of the palate molle and protrusion of tissue from the midline. Palpation if possible to distinguish abscess from cellulitis (Adams, 1997).
In the investigation can be done:
1. Laboratory tests such as complete blood, electrolytes, and blood culture. Which is the "gold standard" for diagnosing abscess peritonsilar is by collecting pus from the abscess using a needle aspiration (Jevuska, 2007).
2. Radiological examination in anteroposterior position only shows "distortion" of the network but not useful for certain locations who abscess (Daley, 2007).
3. On CT scan can be seen on the tonsils hipodens areas that indicate the presence of fluid in the affected tonsils besides that it also can be seen in an asymmetrical enlargement of the tonsils. This examination can help to plan the operation (Daley, 2007).
4. Ultrasound, a technique is simple and noninvasive and can help in distinguishing between cellulitis and the beginning of the abscess. This examination can also determine a more focused selection before surgery and drainage for sure.

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Peritonsiler abscess (PTA / Quinsy) 5

Peritonsiler abscess is an infection that started from the outer surface that extends into the inner layer of soft tissue. Exactly pathophysiology of PTA is unknown. However, several theories attempt to explain the mechanism of the PTA, and the theory was widely accepted that the occurrence of an abscess peritonsiler tonsil inflammation spreading from there. Abscess formed between tonsila Palatina and the capsule, usually in the superior region. It is then believed that the abscesses originated from an acute episode include tonsilits growing soft tissue around the area (Mehta, 2007). Other Mecanisme happened is the emergence of necrosis and pus in the capsular area, which then clog the Weber glands, minor salivary glands found in the living and working peritonsiler help clean up debris from the tonsils, resulting in secretions and forming abscesses (Gosselin, 2008).
Superior and lateral regions tonsilaris fossa is loose connective tissue, the infiltration into the potential supurasi posters peritonsil occupy this area, so look swollen palate molle. In the early stage (stage infiltrates), in addition to swelling, the surface looks hiperemis. If the process continues, the area is more soft and yellowish color. Tonsils pushed to the middle, front and bottom, and swollen uvula pushed to the contralateral side. If the process continues, inflammation of the surrounding tissue will cause irritation of the m. Pterigoid internal, resulting in trismus. Abscesses may rupture spontaneously, may occur to the pulmonary aspiration (Fachruddin, 2002).

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Peritonsiler abscess (PTA / Quinsy) 3

Pharynx is divided into nasopharynx, orofaring and laringofaring. Nasopharynx is part of the pharynx that lies above pallatum molle, which is part orofaring located between palate molle and hyoid bone, while laringofaring part of the pharynx which extends from the hyoid bone to the lower boundary of cartilage crikoid (Ballenger, 1997). Orofaring open to the oral cavity in the anterior pharyngeal pillars. Pallatum molle (vellum palati) consists of muscle fibers are supported by fibrous tissue which is covered by mucosa. Protrusion on the median dividing it into two parts. Forms such as cones, located disentral called uvula. Two columns made up of tonsils tonsilar Palatina anterior and posterior. Glossoplatina and pharyngopalatina muscle is the largest muscle that make up the pillars of the anterior and posterior columns. Tonsils located between the basin palatoglossal and palatopharyngeal (Steyer, 2007).
Plika triangularis (tonsilaris) is a thin fold of mucosa, which covered the anterior pillar and some and some anterior surface of the tonsils. Plika semilunaris (supratonsil) is the upper folds of the mucosa which unites the two pillars. Supra tonsil fossa is the size of the gap varies over the tonsils, located between the anterior and posterior pillars. Tonsil consists of a protrusion of the circular or circular like cripte containing lymphoid tissue and surrounding connective tissue there. Amid the estuary there cripta mucous glands (Ballenger, 1997).
Tonsils and adenoid are the most important part of the Waldeyer ring lymphoid tissue surrounding the pharynx. Tonsils are located in the sinuses tonsilaris between the anterior and posterior pillars faussium. Faussium tonsils are one on each side is orofaring lymphoid tissue that is wrapped by a clear fibrous capsule. The inner surface of the membrane covered by stratified squamous epithelium which is attached. This epithelium extends into the open surface kripta tonsils. Kripta numbered 8-20 on the tonsils, usually tubular and is almost always extends from the tonsils to kekapsul the outer surface of the tonsils. The bound m.konstriktor faringeus superior, so depressed every time swallowing. m. palatoglusus and m. palatofaring also pressing the tonsils.
During the embryonic period, tonsils pharyngeal pouch formed from the second sebegai endodermal bud from the cell. Shortly after birth, tonsils are irregular and grow until it reaches the size and shape, depending on the number of network limphoid (Steyer, 2007).
Structure around tonsilla Palatina (Jevuska, 2007):
1. Anterior
In the anterior part is tonsilla Palatina palatoglossus Arcus, can extend for a short distance below it.
2. Posterior
There posteriorly palatopharyngeus Arcus.
3. Superior
In the superior near palate molle. Here tonsilla joined the lymphoid tissue on the lower surface of palate molle.
4. Inferior
In a third of the posterior inferior tongue. Here, together with tonsilla Palatina tonsilla lingualis.
5. Medial
In the medial part of the oropharynx space.
6. Lateral
There lateral capsula separated from the superior m.constristor pharyngis by loose areolar tissue. V. Palatina externa walked down from the palate molle in this loose connective tissue, to join the plexus venosus pharyngeus. Lateral to the superior pharynges there m.constrictor m. styloglossus and a.facialis arch. A. The internal carotid is located 2.5 cm behind and lateral tonsilla.
Palatina Tonsilla get vascularisasi from: tonsillaris ramus which is a branch of the facialis artery; the branches of a. Lingualis; a. Palatina ascendens; a. Pharyngea ascendens. While innervasinya, obtained from N. Palatinus Glossopharyngeus and minor nerve. Lymph vessels in the nl. Cervicales profundi. The most important node in this group are jugulodigastricus node, which lies below and belakangangulus mandibulae.

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treat melasma : 4 Etiology and Patogenesis

Etiology melasma until now has not been definitely known. According Supardiman (2007), factors that are considered causative role in the occurrence of melasma is patogenesis:

1. Ultraviolet rays.
Spectrum sun damage this cluster sulfhidril in the epidermis which is the enzyme tirosinase resistor with the binding of the enzyme Cu ion is. Ultraviolet rays cause the enzyme tirosinase not dihambat again, so that drive the process of melanogenesis.
Other mechanisms that cause sun exposure can cause melasma is the ultraviolet ray radiation can cause cell membrane lipid peroksidasi so that the generated free radicals stimulate melanosit to release melanin. Curtain especially to block the solar UV-B radiation (290-320 nm) is not satisfactory because there is a wavelength that is longer on the UV-A rays and visible radiation (320-700 nm) have the nature melanosit stimulated to produce melanin.

2. Hormonal
Hormone estrogen, progesteron and MSH can stimulate the formation of melasma.
Hormones have an important role in the human body. On the mask of pregnancy is known in terms obstetrik. Certain mechanisms of melasma because of the pregnancy has not been known. Estrogen level, progesterone, and Melanosit Stimulating hormone (MSH) generally increased in the third trimester. However, in nulipara with melasma, and MSH estrogen level does not increase. Then, the occurrence of melasma because the use of oral contraceptives and diethylstilbestrol used for prostate cancer therapy has also been reported. In the research, women who get menopause will progesteron experiencing melasma, while women who got estrogen not only suffering from melasma, so that it can be proved that progesterone a role in the occurrence of melasma.
One study found that patients with the disease tiroid suffering from melasma. A report of cases also reported that melasma can occur in patients who have experienced emotional stress because of increased MSH produki by hipotalamus.

3. Drugs
For example difenilhidantoin, mesantoin, klorpromasin, sitostatik and minosiklin can cause the occurrence of melasma. Drugs in this collectedthe top of the dermis layer and can stimulate cumulative melanonogenesis.

4. Genetic
Reported cases of family around 20-70%. Genetic factors is a major occurrence of melasma. This occurred mainly in women than men. A person with brown skin and the young sun exposure will increase the excess occurrence of melasma. More than 30% of patients have melasma history of the family who suffered the same aberration. Identical twin trends have also been reported suffering from melasma.

5. Race
Melasma many found in the Hispanic and the dark skin color.

6. Cosmetics
Use of cosmetics that contain perfume, coloring matter or materials that can cause fotosensitivitas which can lead to the emergence hiperpigmentasi in the face if exposed sun.

7. Certain conditions, such as pregnancy and hormone replacement therapy during menopause.

8. Idiopatik.

Pathogenesis melasma is not yet clear, many factors that are considered causative role in pathogenesis melasma.
According Supardiman (2007), pathogenesis the occurrence of melasma involves many factors, such as:

1. Increased production of hormones or because melanosom because ultraviolet rays. Melanosom this increase can also be caused pharmacology materials such as silver and psoralen.

2. Retardation in Malphigian cell turnover. This condition can occur because drugs sitostatika.
Pathogenesis melasma associated with many different fields of science, such as biology, biochemistry, pathology, and patofisiologi process pigmentasi skin, both at the cellular level, biomolekular, skin and tissue. In addition, knowledge of the pathogenesis is very important to establish the diagnosis and treatment.

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juvenil diabetes: 7 etiology and patogenesis

Etiology and Patogenesis
The cause of the basic findings on the initial clinical form of diabetes is dominant at the time the child is secresi of insulin to decrease sharply. Although the degree basalt in plasma insulin can be normal in people with newly diagnosed, insulin production in respon against various secret revealed a strong and usually disappear after many months or many years, rarely exceed 5 years. On certain people who are considered high risk for the development of type 1 diabetes, such as identical twin is not affected by diabetes, a progressive decrease in the capacity as secresi have known for months to many years before showing clinical symptoms of diabetes, which usually become visible at the time of backup secresi insulin or 20% less than normal.
There is evidence indicating that the etiology of diabetes mellitus manifold. Although various types of lesi with different will eventually lead to insulin insufiensi, but the genetic determinan usually play an important role in the majority of people with diabetes mellitus. Insulin dependent diabetes mellitus (DMTI) is a disease that otoimun determined genetic.
Mechanisms that cause the failure of ß cell function of the pancreas to the possibility of damage autoimmune on the islands in the pancreas that have a tendency of individuals. Diabetes mellitus type 1 has long been known to increase in prevalence in people with diseases such as Addison aberration, tiroiditis Hashimoto, and pernicious anemia, which is known autoimun mechanism patogenik. Diabetes mellitus type 1 insulin dependent also be associated with increased frequency of certain HLA, especially HLA-B8,-DR3,-BW15, and-DR4. Located on chromosome 6, the HLA system histokompatibilitas major complex consisting of a group of genes that code transplantation antigen and plays a central role in the immune response.

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juvenil diabetes: 3 blood glucose

Diabetes mellitus is a deficiency causes hormone insulin, which functions utilize glucose as a source of energy and fat sintesa. The result is the cumulative glucose in the blood (hiperglikemia) and finally through the urine without ekskresi used (glycosuria). Therefore, urine production is increased and the patient must urinate often, feeling very thirsty, decreased body weight and feel tired.

Blood glucose
Glukoneogenesis body will meet the interests of glucose at the time of carbohydrate is not available in sufficient amount of glucose in food. Supply continuously required as a source of energy, particularly for the nervous system and eritrosit. Failure on the glukoneogenesis usually fatal result. Blood glucose level below the critical value will cause disfungsi brain that can lead to coma and death. Glucose also needed in the network as adipose source gliseda- glyseril, and may have a role in maintaining the level of compound in the citric acid cycle in the body in many networks. Even in circumstances in which supply most of the fat calorie needs for the organism, the particular needs of basaltic will glucose there. Glucose is one - one of the baker's energy supply for the muscles in order anaerobe. This element is a precursor of milk sugar (lactose) in the breast gland and is actively taken by the fetus. In addition, the mechanism glukoneogenesis in use to clean the various products of metabolism other network in the blood, such as lactate produced by muscle and eritrosit, and glycerol that it continuously produced by the network adiposa. Propionat, namely acid fat glukogenik in the main produce in the process of carbohydrate digest by ruminant animals, is important for substrate glukoneogenesis body in this animal species.
Most of the carbohydrate in food that is most of the glucose will be formed. Carbohydrate foods are digested in the active residues containing glucose, and galaktosa will fruktosa in the offshore in intestinum. Elements in this nutrient transport into the vena porta hepar through hepar. Galaktosa and fruktosa immediately in a change in glucose hepar.

Glucose in the form of various compound glukogenik the glukoneogenesis. This compound can be in the grade in 2 categories:
(1) compound that includes the conversion into glucose net directly without re-cycle, which means, as some amino acids and propionate, and
(2) compound which is a partial result of glucose metabolism in certain network and the in transport in the kidney and hepar for synthesis back into glucose. Thus, the compound that laktat through glucose oxidation in muscle and order by eritrosit, will be taken in hepar and kidney for glucose re-made so that the element is available for circulation through oxidation in the network. This process is known as Cori cycle or cycles lactate acid. Glycerol 3-phosphate for synthesis triasilgriserol network adipose derived from blood glucose. Asilgliserol compound on the network adiposa continue to experience in the hydrolysis to form free gliserol that can not be in use by the network and thus adipose will be diffuse out and into the blood. This free Gliserol will converted into glucose through a mechanism glukoneogenesis in hepar and kidney.
Between acid-amino acid is transported from muscle to hepar in during the famine was the most dominant alanine. This then produces postulate cycle alanine the glucose-glucose recycling result of hepar to muscle with the piruvat, which was followed by transmitting a alanine, and transportation alanine to hepar, and then followed by glukoneogenesis back into glucose. Net transfer of amino nitrogen from muscle to hepar and free energy from the muscles to hepar thus can be done. Energy needed for glucose synthesis in the hepar of piruvat derived from acid-oxidation fatty acid. Also be formed from glucose glycogen hearts through glikogenolisis.

On deficiency insulin there is a heavy acceleration lipolisis. This resulted in the increase rate triasil-gliserol plasma (hiperlipidemia). Few asetil-KoA can metabolise through the citric acid cycle, so the rest must be converted into acid-keto acid (ketonemia) and some excrested(ketonuria). Because glikolisis blocked, enzyme glucose 6-phosphate that the acceleration of glikogenolisis will changed into glucose. This together with the acceleration glukoneogenesis result hiperglikemia (due to increased amino acid and which have increased the amount of enzyme PEPCK). Insulin is basically the reverse of all this. (Murray, 1999)

The process of maintaining a stable glucose level in the blood is one of the homeostasis mechanisms that set the fine and also the one where hepar, network ekstrahepatik and took some hormone. Cell heart cells appear to be passed with a glucose-free (through the GLUT transporter 2), while cells outside the network ekstrahepatik (outside the island of Langerhans pancreas) is relatively not permeable. As a result, crossing through the membrane into the cell phase-speed barrier in the process of glucose in the network ekstrahepatik, glucose and the process fosforilasi quickly by heksokinase at the time of entry in cells. Conversely, enzyme activity and concentration of some compound that may be important to provide a far more direct or to the expenditure of glucose in hepar. However, the concentration of glucose in the blood are important factors that control the speed of glucose in the hepar and ekstrahepatik network. Role of various glikosa the transporter protein found in the cell membrane and each have 12 pieces of transmembran.

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juvenil diabetes: 2 etiology

Epidemiology
DM is a disease with great consequences to health and social. Not only because of the high prevalence of complications, but because cronic and a high death rate.
Prevalence of DM in the world continues to increase. In 1995, prevalence 4.0%. In the year 2025 is estimated to be 5.4%. In developing countries increased prevalence is more light. In 1995 it was found 84 million cases of DM and in the year 2025 this figure will increase to 228 million.
The occurrence of diabetes was 7 years before diagnosis, so morbidity and early mortality occurred in cases that are not detected.

Etiology and Pathogenesis
Developments in understanding the etiology and pathogenesis DM revitedthe previous classification. Although all types of DM by the hyperglycemia, but pathogenesis occurrence hyperglycemia very different. 2005 American Diabetes Association (ADA) to make the classification, the diabetes is type 4, among others, type 1 DM, type 2 DM, type DM, and DM in pregnancy. Diagnostic criteria of DM, according to the ADA in 2005 is:
1. When blood sugar 200 mg / dl if the typical complaints,
2. Fasting blood sugar 126 mg / dl.
3. Plasma glucose level 200 mg / dl at 2 hours after glucose load at 75 grams TTGO.
Diabetes mellitus is not a single form, but presumably is a heterogeneous group of aberration is the difference between the pattern and the genetic mechanism and etiology patofisiologi other disturbances that cause glucose tolerance. National Diabetes Data Group has put the classification category and diabetes glucose intolerance based on the knowledge of the present. This classification has been accepted and supported by various diabetes associations around the world by researchers and Pediatrics. Three main forms of diabetes and some forms of carbohydrate intolerance were identified: Type I Diabetes (Diabetes mellitus Juvenil), type II diabetes, and secondary diabetes.

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hiv - aids 3 pathogenesis

PATHOGENESIS HIV / AIDS

Limfosit CD4 + is the main target of HIV infection because the virus has affinities against the surface of CD4 + molecule. CD4 + Limfosit coordinate the work of a number of important functions immunologist. Loss of function causes disruption of a progressive immune response.
ODHA in the body, the virus particles to join the DNA cell patients, so that once an HIV infection, a life he will remain infected. Of all the people infected with HIV, some developing AIDS in the entry stage 3 year, 50% developed into AIDS patients after 10 years, and after 13 years almost all the people infected with HIV show symptoms of AIDS, and then died. Travel disease shows a picture of chronic diseases, according to the body's immune system impairment is also staged. (Djoerban, 2006)
After entering the blood, HIV will entry in T4 (CD4 +), a part of the integral and infected cells will lead to cell death T4. When most of the T4 have been destroyed will disease symptoms develop. Major core protein with BM / molecular weight of 24,000 (p24), and 2 on the main glikoprotein membrane with BM. BM 41,000 and 120,000 (gp 41 and gp 120), becomes the basis for diagnosis serology's. Most patients infected with HIV can be detected in the circulation of the antibody against primary HIV antigen. HIV infection spread throughout the organ. Body may react in immunologist, and clinical consequences occur aberration, called acute HIV syndrome. This phase lasts relatively short. Virus and is in the latent or concealed, does not cause symptoms. Having the infection can only be known through laboratory testing, detected antibody that is specific to people with HIV in the blood. This phase can take 8-15 years. During this phase the virus continues to multiply in the patients body and in many cells, especially cells in the immune system. AIDS is the terminal phase of HIV infection that has lasted for many years, and any damage of the body immune system. (Rikyanto, 2006)
HIV infection does not immediately show signs or symptoms specific. Some do not show symptoms typical of acute HIV infection, 3-6 weeks after infection. Symptoms that occur are fever, sore swallow, lymph gland swelling, rash, diarrhea, or coughing. After acute infection, HIV infection asymptomatic immediately. The period without symptoms is usually run for 8-10 years. But there is a small group of people who travel it is very fast, can be only about 2 years, and there is also a slow way (non-progressor). (Djoerban, 2006)
During the trip natural HIV disease, people in general do not know that his contract HIV. HIV antibody testing laboratory is the easiest way to find out, and in this phase the virus is rarely found in comparison with the acute phase. But people still infectious or can potentially transmit the virus to others. After the acute phase, people with immune system back to normal and functioning normally, but the viruses multiply, the more immune system cells to become more visible and increase worse. Then people go to the next phase, called callback (Progressive Generalized Lymphadenopathy). In the recent phase limfe gland enlargement occurs, especially in the head and neck. Size gland may swell and wane, and generally take a long time. After the phase of incoming calls phase ARC (AIDS Related Complex). (Rikyanto, 2006)
Phase ARC is a deviation from the set of symptoms that precede clinical AIDS. At this phase aberration body immune system has been significantly decreased. Three prominent clinical symptom is chronic fever, diarrhea chronicles (slim diarrhea). May also be accompanied with opportunist infections, which is the main indicator of AIDS, especially Candidiasis. Element end AIDS diagnostic phase often change the criteria. AIDS is the final phase of HIV infection is marked with various opportunist infections. Direct effect of HIV on organ damage include central nervous system, gut, forming elements of the blood, kidneys, joints and skin. Aberration in the third ARC also caused direct effects of HIV, AIDS on the more serious look. Often happens is that people appear to be fast, old, gray, wrinkled skin, and so forth. (Rikyanto, 2006)

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